Behrooz Niknafs - Immunology Research Center, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Naser Shokrzadeh - Infertility and Reproductive Health Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
Mohammad Reza Alivand - Department of Genetic, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammad Bakhtiar Hesam Shariati - Department of Anatomical Sciences and Histology, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran.

Background: The role of glucocorticoids in implantation has been demonstrated. Objective: This study aimed to evaluate the effect of dexamethasone on endometrial receptivity. Materials and Methods: In this experimental study, ۴۰ BALB/c female mice aged eight wk old weighing approximately ۲۵.۰ ± ۱.۴ gr were used. The mice were divided into four groups (n = ۱۰/each) of control, dexamethasone (۱۰۰ μg/kg, intraperitoneal injection), mammalian target of rapamycin (mTOR) inhibitor (PP۲۴۲) (۳۰ mg/kg, intraperitoneal injection), and dexamethasone and PP۲۴۲. The endometrial epithelium of the mouse was separated to measure messenger RNA expression of heart and neural crest derivatives-expressed protein ۲ (HAND۲), Msh homeobox ۱ (Msx-۱), heparin binding epidermal growth factor (HB-EGF), microRNA (miRNA) Let‐۷a, miRNA-۱۴۵ and miRNA-۴۵۱, using real-time polymerase chain reaction. Also, protein expression of mammalian mTOR and eukaryotic translation initiation factor ۴E‐binding protein۱ (۴E-BP۱) was measured using western blot. Results: The results revealed that the expression of Msx-۱, HAND۲, HB-EGF, miRNA-۴۵۱, and miRNA-Let-۷a was significantly decreased in the endometrium in the dexamethasone group compared to the control, while the expression of miRNA-۱۴۵ in the endometrium was up-regulated. Additionally, the administration of PP۲۴۲, known as an inhibitor of mTOR, was associated with significantly reduced expression of Msx-۱, HAND۲, HB-EGF, miRNA-۴۵۱, and miRNA-Let-۷a, while PP۲۴۲ induced messenger RNA expression of miRNA-۱۴۵. Conclusion: It appears that dexamethasone can diminish uterine receptivity during the implantation period, at least to some extent, through the alteration of particular genes that impact endometrial receptivity. Furthermore, the mTOR pathway seemingly showed an essential role in endometrial receptivity.

Endometrial receptivity, Dexamethasone, HB-EGF, MSX-۱, mTOR, Mouse.